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Oncol Lett. 2016 Jan;11(1):405-410. Epub 2015 Oct 29.

MicroRNA-147 suppresses proliferation, invasion and migration through the AKT/mTOR signaling pathway in breast cancer.

Author information

1
Oncology Center, West China Hospital, Chengdu, Sichuan 610041, P.R. China.
2
Graduate School, Peking Union Medical College and Chinese Academy of Medical Sciences, National Center for Clinical Laboratories, Beijing 100730, P.R. China.

Abstract

The Akt/mTOR pathway is considered to be the most frequently aberrantly activated pathway in human tumors. It is activated in a variety of types of tumor, and is therefore an attractive target for study, including it's potential regulation by microRNAs. A number of microRNAs (miRs) have been demonstrated to target the Akt/mTOR pathway. A previous study reported that miR-147 targets the EGFR-driven cell-cycle protein network in breast cancer. EGFR serves a crucial role upstream to Akt/mTOR. To define the function and mechanism of miR-147 in breast cancer, the present study assessed miR-147 expression in a normal mammary epithelial cell line and three breast cancer cell lines, and observed that miR-147 expression was markedly low in the highly invasive cell line, MDA-MB-231. Ectopic expression of miR-147 in MDA-MB-231 resulted in a reduction of the phosphorylation of crucial molecules in the Akt/mTOR pathway and the proliferation, invasion and migration of the cell line was also reduced. The effects of miR-147 expression are similar to that of shRNA which is specifically designed to silence the expression of Akt. The findings of the present study indicate that miR-147 suppressed the proliferation, invasion and migration of breast cancer cells through targeting the Akt/mTOR signaling pathway. As a new microRNA targeting Akt/mTOR pathway. Using miR-147 may therefore provide an effective therapeutic approach to suppress tumorigenicity in breast cancer.

KEYWORDS:

Akt/mTOR pathway; breast cancer; invasion; microRNA; migration; proliferation

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